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Renal 2 > Robbins Ch. 20 - Cysts, Obstruction, Neoplasia > Flashcards

Robbins Ch. 20 - Cysts, Obstruction, Neoplasia Flashcards

1
Q

Kidney agenesis must be ____ to survive

What else will you see?

A

UNILATERAL

Compensatory enlarging of solitary kidney

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2
Q

Most common site of ectopic kidney?

Complication?

A

Pelvic brim or within pelvis

Ureteral kinking/tortuosity –> obstructed flow

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3
Q

Locations of renal colic

A

12th rib costovertebral angle (CVA) to groin

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4
Q

Unilateral cystic, enlarged kidney
Abdominal mass on palpation
Undifferentiated mesenchyme pockets with cartilage
Other GU abnormality (missing ureter, obstruction, etc.)

A

Multicystic renal dysplasia

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5
Q

Bilateral enlarged, multicystic kidneys
Hematuria –> proteinuria, polyuria, HTN
Adult

A

Autosomal dominant (Adult) polycystic kidney disease

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6
Q

ADPKD patients can often have what other congenital anomalies?

A

Liver cysts, berry aneurysms, mitral valve prolapse, HTN coronary/heart disease

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7
Q

ADPKD genetics

A

PKD1 (polycystin-1) or PKD2 (polycystin-2) gene mutations

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8
Q

Enlarged, smooth, sponge-like kidneys

Neonate with kidney failure

A

Autosomal recessive (childhood) polycystic kidney disease

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9
Q

ARPKD patients often have what else?

A

Portal and systemic HTN, hepatic fibrosis

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10
Q

ARPKD genetics

A

PKHD1 gene deficiency (fibrocystin)

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11
Q 
Cysts at the corticomedullary junction
Shrunken kidneys
Chronic tubulointerstitial nephritis
Child
Polyuria, polydipsia
Growth retardation
A

Familial juvenile nephronophthisis

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12
Q

Genetics of FJN

A

Autosomal recessive - NPHP gene mutations

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13
Q

Expected outcome for FJN

A

ESRD in 5-10 years

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14
Q 
Cysts at the corticomedullary junction
Shrunken kidneys
Chronic tubulointerstitial nephritis
Adult
Polyuria, polydipsia
A

Adult-onset nephronophthisis

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15
Q

Genetics of adult-onset nephronophthisis

A

Autosomal dominant - MCKD gene mutations

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16
Q

Expected outcome for adult-onset nephronophthisis

A

Chronic renal failure

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17
Q

Only medullary cystic disease WITHOUT an inheritence pattern

A

Medullary sponge kidney

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18
Q

Adult
Normal renal function
Collecting ducts are dilated (grossly)
Small cysts lined with epithelium in medulla

A

Medullary sponge kidney

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19
Q

Patient on chronic dialysis

Cortical and medullary cysts/stones

A

Acquired cystic disease (dialysis-associated)

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20
Q

Acquired cystic disease:

Renal stones made of ____
Risk for developing ____

A

Calcium oxalate

Renal cell carcinoma

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21
Q

Microscopic hematuria
Cortical cyst(s)
Normal-sized kidneys

Clinical outcome?

A

Simple cysts

Benign

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22
Q

Teenager/young adult with GENETIC form of ESRD…

Most likely to be what?

A

Familial/juvenile nephronophthisis

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23
Q

Obstructive lesions increase risk of ____

A

Infection and stone formation

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24
Q

Chronic unrelieved obstruction leads to ____

A

Renal atrophy (Hydronephrosis, Obstructive uropathy)

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25
Q

Hydronephrosis

A

Dilation of renal pelvis and calyces due to atrophy of kidney due to urine outflow obstruction

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26
Q

Renal colic (pain in lower thoracic and lumber)
Bladder symptoms
Distention of collecting system

A

Acute obstruction

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27
Q 
Urinates a lot
Urinates at night
Hypertension
Renal calculi
Tubulointerstitial nephritis
A

Bilateral partial obstruction

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28
Q

Male, 20s, intense unilateral renal colic

Increased urinary concentration of certain molecule (supersaturation of it)

A

Nephrolithiasis

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29
Q

Causes of calcium oxalate stone formation

A

Hypercalciuria via…

  • Hypercalcemia
    - Hyperparathyroidism
    - Diffuse bone disease
    - Hyperabsorption by intestine
    - Sarcoidosis
  • Idiopathic hypercalciuria (w/o hypercalcemia)
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30
Q

Bacterial infection
Large renal stones in renal pelvis

Most likely bacteria? (3)

A

Magnesium ammonium phosphate stones

Urea-splitters (Proteus, Klebsiella, Staph)

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31
Q

Does having uric acid stones indicate hyperuricemia or excess excretion of uric acid?

A

NOT ALWAYS -

32
Q

4 influencing factors for calculi formation

A
  • Increased concentration of constituents
  • Urinary pH change
  • Decreased urinary volume
  • Bacterial infection
33
Q

Most common renal neoplasm

A

Renal papillary adenoma

34
Q

Small, well-circumscribed nodule in the renal cortex made of complex branching with papillary fronds. Found to be of epithelial origin.

Prognosis?
Genetics?

A

Renal papillary adenoma

Benign (if less than 3 cm)
Trisomy 7 or 17

35
Q

Adult
LARGE (12 cm) renal tumor with large eosinophilic cells w/ numerous mitochondria
Tan/brown, well-encapsulated, central scar

Important differential Dx?
Malignant?

A

Oncocytoma

Non-clear cell renal cell carcinoma

Benign

36
Q

Adult female
(Retroperitoneal hemorrhage, shock)
Renal tumor with vessels, muscle, and fat
Skin abnormalities, neurologic symptoms, other tumors (heart, etc.)

Most likely genetic mutation?
Hereditary pattern?

A

Angiomyolipoma

TSC1 or TSC2 (TUBEROUS SCLEROSIS)
- Autosomal dominant

37
Q

Easy way to know an angiomyolipoma on pathology presentation

A 
Thick blood vessels ("angio")
Smooth muscle ("myo")
Fat vesicles ("lipoma")
38
Q

Older adult, smoker
Costovertebral pain
Palpable renal mass
Hematuria

A

Renal cell carcinoma

39
Q

Familial forms of renal cell carcinoma

A
  • Von Hippel-Lindau
  • Hereditary leiomyomatosis/renal cell cancer
  • Hereditary papillary carcinoma
  • Birt-Hogg-Dubé syndrome
40
Q

Biggest risk factor for renal cell carcinoma

A

TOBACCO

41
Q

Non-papillary unilateral unifocal renal tumor
Chr. 3 (VHL) deletion
Proximal tubular epithelium

A

Clear cell carcinoma

42
Q

Pathophysiology of clear cell carcinoma

A

Low VHL = high HIF-1 = high VEGF, IGF-1

43
Q

Papillary multifocal renal tumors
Trisomy 7, 17
Mutated (active) MET gene

A

Papillary carcinoma

44
Q

Renal tumor w/ pale eosinophilic cytoplasm and nuclear halos
Similar to oncocytoma

Prognosis?

A

Chromophobe renal carcinoma

GOOD prognosis (compared to clear cell and papillary)

45
Q

Clear cell carcinomas have mutations on what chromosome?

A

Chr. 3

46
Q

Papillary cell carcinomas have mutations on what chromosome?

A

Chr. 7

47
Q

Genetic difference between sporadic and hereditary papillary renal cell carcinomas

A

Sporadic - Trisomy 17 + loss of Y chromosome ALSO

48
Q

Xp11.2 translocation (TFE3 gene)

Clear cytoplasm, papillary architecture

A

Xp11 translocation carcinoma

49
Q

RCC metastasizes where?

A

Renal vein, lung, bone, other

50
Q

Systemic importance of RCC

A

Many paraneoplastic syndromes of metastases (polycythemia, hyperCa++, HTN, sexual changes, cushings, eosinophilia, amyloidosis, etc.)

51
Q

Rate RCCs by prognosis (6 total)

A

Good: papillary and chromophobe
OK: clear cell
Bad: collecting duct, sarcomatoid, medullary

52
Q

Typical location of RCC within kidney

A

Upper pole

53
Q

Diagnosing clear cell carcinoma

A

Positive Oil Red-O stain

54
Q

Why are clear cells clear?

A

Glycogen and LIPID elaboration

55
Q

RCC, spindle cells (like mesenchymal)

A

Sarcomatoid RCC

56
Q

RCC, branching tubules w/ cuboidal cells

A

Collecting duct carcinoma

57
Q

RCC, sickle cell disease

A

Medullary carcinoma

58
Q

Gross hematuria
Palpable hydronephrosis
Flank pain
Smoker

Most likely locations?

A

Urothelial (transitional cell) carcinoma

Renal pelvis AND BLADDER

59
Q

Prognosis of urothelila carcinoma

A

Bad

60
Q

4 most common childhood MALIGNANT tumors

A
  1. Acute leukemia
  2. Neuroblastoma
  3. Retinoblastoma
  4. Wilms tumor
61
Q

Child, 2-5 y/o
Large abdominal mass (unilateral usually)
Pain, microscopic hematuria, HTN
Metastatic

A

Wilms tumor (nephroblastoma)

62
Q

Familial syndromes w/ wilms tumor

A

WAGR (wilms-aniridia-genital-retardation)
Denys-drash syndrome (gonadal and renal)
Beckwith-Wiedemann syndrome

63
Q

Percentage of wilms tumors that are congenital/genetic

A

10%

64
Q

WAGR and DDS have what mutation?

A

Chr. 11 (WT1 gene)

65
Q

B-W syndrome has what mutation?

A

None or WT2

66
Q

Wilms tumor

Hypertrophy of one half of body

A

Beckwith-Wiedemann syndrome

67
Q

Wilms tumor
Mental retardation
No colored portion of eye

A

WAGR syndrome

68
Q

Wilms tumor

Gonadal tumor

A

Denys-Drash syndrome

69
Q

Wilms tumor + nephrogenic rests –> suspect what?

A

BILATERAL + MULTIPLE tumors

70
Q

2 morphologies of wilms tumor

A
  • Triphasic (blastema, epithelial (tubular), stromal)

- Anaplastic (pleomorphism and atypia)

71
Q

Anaplastic wilms tumor…

- 2 things to note

A
  1. p53 mutation

2. Resistant to chemo

72
Q

Location and morphology of wilms tumor

A

Lower pole
Tan/gray color
Well-circumscribed

73
Q

Prognosis of wilms tumor

A

GOOD - curable

74
Q

How to genetics and age relate to prognosis of wilms tumor?

A

p53 (anaplastic), gene mutations = WORSE

Younger age = WORSE

75
Q

Most common metastases TO the kidneys

Locations?

A

Small cell lung

Bilateral, multifocal

Renal 2 (11 decks)

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